CCN1 Induces Oncostatin M Production in Osteoblasts via Integrin-Dependent Signal Pathways
| Autor: | Cheng-Yu Chen, Lih-Jyh Fuh, Yuan-Li Huang, Chen-Ming Su, Chih-Hsin Tang, Chun-Hao Tsai |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Chromatin Immunoprecipitation
Integrins Immunology Blotting Western Integrin lcsh:Medicine Rheumatoid Arthritis Enzyme-Linked Immunosorbent Assay Oncostatin M Real-Time Polymerase Chain Reaction Autoimmune Diseases Cell Line Extracellular matrix Focal adhesion Phosphatidylinositol 3-Kinases Cell Signaling Rheumatology Medicine and Health Sciences Humans Medicine lcsh:Science Immune Response PI3K/AKT/mTOR pathway Phosphoinositide-3 Kinase Inhibitors Inflammation Osteoblasts Multidisciplinary biology business.industry Arthritis lcsh:R NF-kappa B Biology and Life Sciences Cell Biology Cell biology Focal Adhesion Protein-Tyrosine Kinases CYR61 biology.protein Phosphorylation lcsh:Q Clinical Immunology Oncostatin M production business Research Article Signal Transduction Cysteine-Rich Protein 61 |
| Zdroj: | PLoS ONE PLoS ONE, Vol 9, Iss 9, p e106632 (2014) |
| ISSN: | 1932-6203 |
| Popis: | Inflammatory response and articular destruction are common symptoms of osteoarthritis. Cysteine-rich 61 (CCN1 or Cyr61), a secreted protein from the CCN family, is associated with the extracellular matrix involved in many cellular activities like growth and differentiation. Yet the mechanism of CCN1 interacting with arthritic inflammatory response is unclear. This study finds CCN1 increasing expression of oncostatin m (OSM) in human osteoblastic cells. Pretreatment of αvβ3 monoclonal antibody and inhibitors of focal adhesion kinase (FAK), c-Src, phosphatidylinositol 3-kinase (PI3K), and NF-κB inhibited CCN1-induced OSM expression in osteoblastic cells. Stimulation of cells with CCN1 increased phosphorylation of FAK, c-Src, PI3K, and NF-κB via αvβ3 receptor; CCN1 treatment of osteoblasts increased NF-κB-luciferase activity and p65 binding to NF-κB element on OSM promoter. Results indicate CCN1 heightening OSM expression via αvβ3 receptor, FAK, c-Src, PI3K, and NF-κB signal pathway in osteoblastic cells, suggesting CCN1 as a novel target in arthritis treatment. |
| Databáze: | OpenAIRE |
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